Flagellin preserves eosinophils in the gut

Long non-coding RNA (lncRNA) LUCAT1 has recently been recognized as an oncogene in several malignancies. This study was launched to probe its role in thyroid carcinoma (TC) development and the implicated molecules.
LUCAT1 expression in TC cell lines and in normal thyroid follicular epithelial cell line Nthy-ori3-1 was determined by RT-qPCR. Binding relationships between LUCAT1 and microRNA (miR)-493, and between miR-493 and a disintegrin and metalloproteinase-10 (ADAM10) were predicted on a bioinformatics system and then validated through luciferase reporter gene assays. Expression of miR-493 and ADAM10 in TC cells was determined. Gain- and loss-of functions of LUCAT1, miR-493 and ADAM10 were performed to explore their influences on the behaviors of TC cells. Xenograft tumors were induced in nude mice for in vivo studies.
LUCAT1 and ADAM10 were highly expressed, while miR-493 was poorly expressed in TC cell lines. LUCAT1 served as a miR-493 sponge to upregulate ADAM10 expression. Silencing of LUCAT1 discouraged proliferation, invasion, and migration but triggered apoptosis of TC cells. By contrast, these changes were abrogated by further miR-493 inhibition or ADAM10 upregulation. The in vitro experiment results were reproduced in vivo. In addition, miR-493 inhibition or ADAM10 overexpression was found to increase the phosphorylation of STAT3 in cells.
This study evidenced that LUCAT1 increases ADAM10 expression through sequestering miR-493, leading to JAK-STAT activation and TC cell growth and metastasis. LUCAT1 and ADAM10 may serve as therapeutic targets for TC treatment.
This study evidenced that LUCAT1 increases ADAM10 expression through sequestering miR-493, leading to JAK-STAT activation and TC cell growth and metastasis. LUCAT1 and ADAM10 may serve as therapeutic targets for TC treatment.
Renal artery stenosis leads to ischemic renal insufficiency, but methods for assessing renal perfusion are limited. This study aimed to evaluate the association between renal slow perfusion and impaired renal function in atherosclerotic renal artery stenosis (ARAS).
A total of 79 consecutive patients with uncontrolled hypertension who underwent renal angiography and renal dynamic scintigraphy for suspected ARAS were enrolled in the retrospective descriptive study. Based on the status of renal artery stenosis and renal perfusion, participants were divided into three groups the control group (n=26), the unilateral ARAS with renal normal perfusion group (RNP, n=30), and the unilateral ARAS with renal slow perfusion group (RSP, n=23). RSP was defined as renal blush grade (RBG) ≤1, while RBG>1 belonged to RNP. Split renal function (SRF) was achieved from 99mTc-DTPA renal scintigraphy. The value of the difference in split renal function (DSRF) is contralateral SRF minus impaired SRF of paired kidneys in ARAS. We compared the SRF and DSRF between different groups to identify the association between renal slow perfusion and renal impairment in ARAS.
We analyzed SRF for paired kidneys and found the following (1) The SRF of the paired kidney was similar in the RNP group (24.3 ± 10.2 mL/min vs 27.5 ± 8.4 mL/min;
= 0.19); however, the impaired SRF was obviously decreased compared with the contralateral SRF in the RSP group (13.5 ± 8.6 mL/min vs 36.7 ± 16.9 mL/min;
< 0.001); and (2) The difference in SRF in the RSP group was significantly higher than that in the control and RNP groups (19.8 ± 11.9 mL/min vs 4.8 ± 8.1 mL/min; 19.8 ± 11.9 mL/min vs 4.6±3.7 mL/min;
< 0.05).
As an angiographic phenomenon, renal slow perfusion might be an indicator of severely impaired renal function.
As an angiographic phenomenon, renal slow perfusion might be an indicator of severely impaired renal function.Cerebral fat embolism (CFE) causes the neurological involvement observed in fat embolism syndrome, which is a post-traumatic complication seen mostly after long bone fractures and usually presents 24-72 h after the injury. An early 80s female who sustained an isolated traumatic fracture of the left distal femur without dislocation was alert on admission but fell into a coma 55 min after the injury. Brain computed tomography showed no abnormalities. Brain magnetic resonance imaging was performed approximately 5 h after the accident, and diffusion-weighted images revealed hyperintense, dot-like lesions disseminated in a "starfield" pattern in the brain. Selleck Tunicamycin The patient was diagnosed with CFE and admitted to the intensive care unit. The day after the injury, the patient developed petechiae on the palpebral conjunctiva and was still comatose 4 months after the trauma. The current patient developing CFE in less than 1 h after a traumatic injury illustrates that CFE should be considered in patients with sudden deterioration of consciousness within 1 h after long bone fractures.Here, we report a case of a patient with symptoms of Cushing syndrome, who is diagnosed with primary generalized glucocorticoid hypersensitivity in the end. The patient's relevant laboratory tests and imaging examinations are described. Mifepristone, a glucocorticoid receptor antagonist, was prescribed and its therapeutic effect on the patient's electrolyte level, lipid metabolism, and bone metabolism was observed during the treatment. The endocrine assessment indicated normal pituitary-adrenal axis regulation function but reduced cortisol secretion. Quantitative reverse transcription-polymerase chain reaction indicated reduced mRNA level of mineralocorticoid receptor gene. Pituitary magnetic resonance imaging showed normal pituitary anatomy, while adrenal computed tomography scan showed bilateral adrenal atrophy and increased content of visceral and abdominal subcutaneous fat. Moreover, chromosome examination revealed a normal 46, XY chromosome. In this case, mifepristone was administered to treat primary generalized glucocorticoid hypersensitivity. To the best of our knowledge, there are a few reports on mifepristone-treated primary generalized glucocorticoid hypersensitivity. In the one-year follow-up visits, the evaluated results of electrolyte level, lipid metabolism, and bone metabolism indicated that the patient's symptoms resulting from cortisol hypersensitivity were relieved progressively.